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Gynae Flashcards

1
Q

History of lower abdominal pain.

Distorted fallopian tube, no normal tube present, distended and filled with thin fluid. NO PUS. The wall has become paper thin and the fimbrae are not visible as they have become embedded within the blocked tube.

A

hydrosalpinx

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2
Q

Where does the fluid come from in a hydrosalpinx?

A

The ends of the tube are blocked, and as a result, the tube becomes filled with the thin fluid secretions from the tubal epithelial cells.

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3
Q

What is PID?

A

Pelvic inflammatory disease. Includes infection and inflammation of the upper female genital tract: endometritis, salpingitis, oophoritis

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4
Q

Cause of hydrosalpinx

A

Normally follows PID, more specifically acute salpingitis

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5
Q

Who gets PID?

A
  • 1 in 50 sexually active women in UK/year

- typically women under the age of 25 yrs

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6
Q

Causes of PID

A
  • commonly a result of ascending infection within the genital tract (STI)
  • medical/surgical intervention e.g. hysteroscopy, and certain organisms are associated with the presence of an IUCD (Actinomycetes)
  • TB (spreads via the haematogenous route to the fallopian tubes)
  • Chlamydia trachomatis
  • Neisseria gonorrhoea
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7
Q

IUCD

A

Intrauterine Contraceptive Device

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8
Q

What’s the most common sexually transmitted infection in England?

A

Chlamydia trachomatis

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9
Q

How does a hydrosalpinx develop after an acute infection?

A
  • formation of a pyosalpinx during the acute infection
  • The fimbrial end of the tube is blocked due to inflammation, hence the pus cannot escape.
  • inflammation resolves, the pus is reabsorbed, but the tube remains blocked and a hydrosalpinx develops.
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10
Q

What is a pyosalpinx?

A

a tube distended with pus

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11
Q

Complications of PID

A
  • development of a tubo-ovarian abscess in the acute stages, which may rupture

Longer term they may develop chronic PID with pelvic pain, and this may be complicated by further episodes of acute salpingitis. Serious long term complications are ectopic pregnancy, and tubal infertility:

1 episode of acute salpingitis increases the risk of ectopic pregnancy 7-10 times.

Infertility occurs in approximately 10% patients after 1 episode of PID, but the rate reaches 40 - 75% after 3 episodes.

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12
Q

Presentation of acute salpingitis

A

vague lower abdominal/pelvic pain, often with purulent vaginal discharge, and with or without fever and systemic features of inflammation. However, it is often a silent disease that presents with complications

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13
Q

What’s the problem with acute salpingitis?

A

Often silent presentation so you don’t treat with antibiotics.

Therefore preventative measures include:

  • barrier contraception is important
  • National Chlamydia Screening Programme in the UK, that offers opportunistic non-invasive (urine or vulvo-vaginal swab) chlamydia testing to men and women under the age of 25 yrs.
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14
Q

35-year-old female who presents with acute severe right iliac fossa pain, and vaginal bleeding. History of 8 weeks of amenorrhoea. Cystic structure within the ovary. Tube is distended with a blood clot

A

A tubal ectopic pregnancy

Cystic structure is the corpus luteum

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15
Q

What proportion of pregnancies are ectopic?

A

1%

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16
Q

What is an ectopic pregnancy?

A

Ectopic pregnancy refers to the implantation of the fertilised ovum anywhere other than the uterus.

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17
Q

Common sites for ectopic pregnancies

A
  • 90% of cases fallopian tube
  • ovary
  • uterine cornu (site at which fallopian tube enters the uterus)
  • cervix
  • abdominal cavity (if the fertilised ovum drops out of the fimbrial end of the tube)
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18
Q

What causes a haematosalpinx?

A

The fertilised ovum implants into the wall of the fallopian tube. The developing placenta implants onto the wall of the tube and gradually invades through the wall, as there is no decidua between the placenta and the wall of the tube. The result is haemorrhage into the tube (due to rupture of vessels in the wall) which is referred to as haematosalpinx.

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19
Q

How might an ectopic pregnancy be fatal?

A

Ruptured ectopic pregnancy

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20
Q

How could you confirm a diagnosis of a tube ectopic pregnancy prior to surgery?

A
  • Amenorrhoea suggests pregnancy
  • pregnancy test or serum βHCG would have confirmed this
  • distended tube would have been visible on ultrasound scan (abdominal or transvaginal)
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21
Q

Risk factors for ectopic pregnancies

A

Anything that prevents the fertlised ovum entering the uterus, or that impairs implantation.

However, half of affected women have no predisposing factors.

Risk factors include:

  • Previous salpingitis and PID
  • tubal structural anomalies (which may follow surgery to the tube, pelvic adhesions e.g. secondary to endometriosis (distorting the tube)
  • some fertility drugs
  • uterine abnormalities that prevent passage of ovum into uterus, e.g. distortion by fibroids
  • IUCD (specifically the progesterone releasing IUD, although if pregnancy occurs with a traditional IUD it is more likely to be ectopic)
  • increasing maternal age
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22
Q

What does the corpus luteum do during pregnancy?

A

It is the source of oestrogen and progesterone secretion during the first 12 weeks of pregnancy, under the influence of HCG secreted by the developing placenta (after the 12th week, the placenta takes over the function of the corpus luteum, which then regresses). The oestrogen and progesterone maintain the endometrial lining of the uterus.

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23
Q

Differential diagnosis of acute severe lower abdominal pain (in a woman of reproductive age) are:

A
  • Acute salpingitis
  • Torted ovary and fallopian tube
  • Endometriosis (but not usually acute in onset). May have rupture of an endometriotic cyst.
  • Mittelschmerz (pain associated with ovulation - can be severe)
  • And non-gynaecological causes such as: (this list is not exhaustive)
    Cystitis, ureteric stone, acute appendicitis, diverticulitis

Even in the absence of the history of amenorrhoea, any women of child-bearing age who presents with abdominal pain of this nature should have a pregnancy test to exclude ectopic pregnancy.

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24
Q

What could cause a fallopian tube and ovary that are dark brown/black in colour? Associated with severe lower abdo pain

A

A torted ovary and fallopian tube.

Dark colour due to haemorrhage and infarction (with necrosis) of the tissue. The blockage of venous return due to rotation of the tube and ovary around the broad ligament has resulted in ischaemia and infarction. The structures are also swollen due to oedema.

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25
Q

Which side is it more common to get a torted ovary?

A

Right as the left side is less mobile in the presence of the sigmoid colon.

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26
Q

Risk factors for tortion

A

Enlargement of the ovary regardless of cause:

Tumour (benign or malignant) - involved in 50-60% of cases of torsion
Most commonly a dermoid cyst. Malignant tumours may be associated with adhesions that reduce the likelihood of torsion.

Cyst - of any type, including tumour (see above)
Torsion of the ovary during pregnancy may be due to a corpus luteal cyst or to increased mobility of the ovaries due to general laxity of the ligaments

Developmental abnormality
Torsion of the ovary may be seen in a child. This usually occurs with a normal ovary in association with an abnormality of the fallopian tube (e.g. excessively long tube)

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27
Q

Types of ovarian cysts

A

Ovarian cysts can be functional, endometriotic, or neoplastic. The neoplastic cysts may be benign or malignant (or of borderline malignant potential if epithelial in origin). The more common examples of each are:

Functional cysts: follicular, corpus luteal cysts
Endometriotic (chocolate) cyst: associated with endometriosis

Neoplastic cysts:
Benign: epithelial - mucinous and serous cystadenoma
germ cell tumour - dermoid cyst (cystic teratoma)
Malignant: epithelial - mucinous and serous cystadenocarcinoma
(malignant germ cell tumours are often solid)

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28
Q

Ovaries from female, early twenties, vague abdominal pain with a palpable adnexal mass on examination, cyst wall is smooth and shiny on the outer surface (peritoneal/serosal surface). The lining of the cyst is slightly roughened in areas, noules in the wall, a small amount of hair, and several teeth, cyst is unilocular.

A

mature cystic teratoma aka a dermatoid cyst

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29
Q

What cells do teratomas arise from?

A

Post meiotic germ cells which are totipotential, which means that they have the ability to differentiate along all 3 cell lines (i.e. ectodermal, endodermal, or mesodermal).

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30
Q

What’s the most common germ cell tumour of the ovary, representing around 25% of ovarian neoplasms?

A

Mature cystic teratoma

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31
Q

Who gets teratomas?

A

They are most commonly diagnosed during reproductive life (peak age 20-29 years), and are usually unilateral.

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32
Q

Why are teratomas also known as dermatoid cysts?

A

Almost all teratomas have ectodermal differentiation, and often they contain tissues from the other cell lineages. Commonly, the cysts are lined by skin with its appendages, such as hair follicles and sebaceous glands. It is for this reason that these tumors are sometimes referred to as dermoid cysts.

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33
Q

Prognosis for patients with teratomas

A

These tumours are benign. As such they are confined to the ovary, and once removed the patient is cured. They may undergo torsion (17% of cases) which often results in acute presentation.

Very occasionally (1%), a malignancy may arise within a mature teratoma. This is most often a squamous cell carcinoma arising in the skin component of the tumour.

Less common are the immature teratomas. These are solid tumours, and are considered to be malignant. Mature tissue elements may be seen, but these tumors contain immature tissues, usually ectodermal and mesodermal in origin. The tissues do not have the organised structure that is seen in mature teratomas. The immature neural component is particularly significant.

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34
Q

Types of ovarian tumours

A

Epithelial tumours
Germ cell tumours
Sex cord/ Stromal tumours
Metastatic tumours

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35
Q

What are the epithelial tumours that occur in the ovary?

A

Serous and mucinous ovarian tumours
The surface epithelium undergoes metaplasia (under conditions of repeated damage with ovulation) to give rise to serous and mucinous ovarian tumours. These are often cystic, and they can be benign (cystadenoma; the majority) or malignant (cystadenocarcinoma).

There is a 3rd group of epithelial tumours referred to as those of borderline malignant potential. These are less common, and behave as a low grade cancer.

Other epithelial tumours include endometrioid-type, clear cell (both usually malignant), and Brenner tumour (with urothelial differentiation, and mostly benign).

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36
Q

What’s the most common type of ovanian tumour?

A

Epithelial tumours

Serous tumours representing 30% ovarian tumours.
Mucinous tumours represent 25% of ovarian tumours.
Endometrioid tumours represent 25% of ovarian tumours.

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37
Q

What’s a Brenner tumour?

A

urothelial differentiation, and mostly benign

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38
Q

Second most common ovarian tumours

A

Germ cell tumours

Of these, the teratoma is the most common

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39
Q

Malignant germ germ cell tumours

A

DECY

dysgerminoma
embryonal carcinoma
choriocarcinoma
yolk sac tumour (endodermal sinus carcinoma)

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40
Q

Are sex cord/stromal tumours benign or malignant?

A

Most benign

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41
Q

Most common Sex cord/stromal tumour

A

Fibroma/thecoma.

The thecoma component can be hormone (oestrogen) secreting, and may give rise to endometrial abnormalities.

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42
Q

Which sex cord/stromal tumours may secrete androgens or oestrogens?

A

Granulosa cell tumour, and Sertoli-Leydig tumour

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43
Q

Small cysts are known as

A

Locules

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44
Q

Pathology of mucinous and serous tumours

A

With repeated ovulation during reproductive life, the surface of the ovary becomes scarred, and with time the epithelium becomes embedded in the ovarian cortex in the form of small cysts. The lining of these cysts can undergo metaplasia, most commonly to serous or mucinous type, to give rise to serous and mucinous ovarian tumours respectively. This is thought to be due to increased susceptibility to genetic mutations during repeated episodes of epithelial damage and repair.

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45
Q

Term for benign cyst tumours

A

Cystadenomas

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46
Q

Term for malignant cyst tumours

A

Cystadenocarcinomas

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47
Q

What are borderline malignant tumours?

A

These are less common than mucinous/serous epithelial tumours

Generally behave as a low grade cancer, and some may have peritoneal involvement.

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48
Q

Malignant epithelial tumours

A

endometrioid-type,

clear cell

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49
Q

Features of benign mucinous tumours

A
  • smooth serosal surface over the ovary

- intact capsule

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50
Q

What are fibroids also known as?

A

Leiomyomas (leiomyosarcomas if malignant)

They are tumours of smooth muscle which commonly arise in the myometrium.

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51
Q

What’s the 4th most common malignancy in UK females?

A

Ovarian cancer (after breast, bowel, and lung).

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52
Q

Most common cell type of malignant ovarian tumours

A

epithelial in origin

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53
Q

Who gets ovarian tumours and what’s the prognosis?

A

rarely diagnosed in women <40yrs old.

These tumours have a relatively poor prognosis in comparison with other malignancies of the female genital tract simply because they usually present late due to non-specific clinical features.

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54
Q

Benign or malignant?

Solid areas on the surface of the ovary which have a cauliflower-like appearance which is referred to as ‘papillary’. There are several cysts present which have been sliced to reveal thick tan greasy (mucinous) contents.

A

On the surface= malignant

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55
Q

Risk factors for ovarian cancer

A

Increased age: most malignant ovarian tumours occur in post-menopausal women

Positive family history: 1 in 20 ovarian malignancies is seen in a patient who has a positive family history. In some of these cases the tumours will have arisen in association with an inherited gene mutation, such as BRCA 1, or HNPCC (hereditary non polyposis colon cancer syndrome). These tumours usually occur at a younger age (those patients with known inherited mutation in BRCA 1 may be screened for the development of ovarian cancer).

Early menarche/late menopause, nulliparity: related to the number of ovulatory cycles (during pregnancy there is no ovulation).

Protective factors: Breast feeding and the oral contraceptive (both by suppressing ovulation).

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56
Q

Ten year survival rate of malignant serous tumours

A

10-20%

57
Q

Ten year survival rate of malignant mucinous tumours

A

35%

58
Q

Prognosis of endometrioid tumours compared to mucinous and serous tumours

A

Better as tend to present at an earlier stage

59
Q

What’s Meigs syndrome?

A

Meigs syndrome is defined as the triad of benign ovarian tumor (fibroma) with ascites and pleural effusion that resolves after resection of the tumor. Ovarian fibromas constitute the majority of the benign tumors seen in Meigs syndrome.

60
Q

Bilateral, ovaries enlaged and composed of mucin containing signet ring cells in dense fibrous stroma

A

Krukenberg tumour (a metastatic tumour usually from the stomach, colon or breast)

61
Q

Clinical staging for ovarian tumours and 5 yr survival

A

FIGO International Federation of Gynecology and Obstetrics

I Limited to ovaries
Ia One ovary, no ascites 85%
Ib Both ovaries, no ascites 40% 
Ic Malignant ascites 40%
II Pelvic extension 40%
III Intraperitoneal spread (omentin, liver, spleen) 15%
IV Distant metastases <5%
62
Q

Ovary which is grossly enlarged and has been replaced by tumour. There is a short length of normal fallopian tube attached to the ovary. The ovary was removed from a 39 yr old female. Her other ovary was normal.

The surface of the ovary is smooth and shiny. The cut surface of the tumour has a white/cream homogenous whorled appearance. There are no cystic spaces. There is no haemorrhage or necrosis. There is no residual normal ovary visible.

A

ovarian fibroma

63
Q

What’s the most common subtype of sex cord/stromal tumour (representing two-thirds of these tumours), and account for 6% of ovarian tumours?

A

Ovarian fibromas. Most are benign

64
Q

Who gets fibromas?

A

usually seen in women 20-80 years of age, with an average age of >50 years.

65
Q

Presentation of fibromas

A

They may be an asymptomatic, and an incidental finding, or presentation may be with vague abdominal discomfort if the tumour reaches a large size. These tumours may grow to an excess of 10cm in diameter as seen here. These large tumours may present with ascites (40% tumours >10cm have associated ascites).

66
Q

Complications of sex cord/stromal tumours

A

hormone secretion, which may lead to their clinical presentation:

Thecomas often secrete oestrogen. This may have a proliferative effect on the endometrium. As such it is a recognised cause of post-menopausal bleeding and may cause irregular menstruation in pre-menopausal women. In a small number of these patients endometrial carcinoma may develop. Oestrogen secretion occurs to a lesser extent in the combined thecoma/fibroma.

Granulosa cell tumours may also secrete oestrogen.

Sertoli-Leydig cell tumours often secrete androgens, which may have a virilising effect.

67
Q

What does virilising mean?

A

the abnormal development of male sexual characteristics in a female

68
Q

How do Krukenberg tumours get to the ovaries?

A

‘transcoelomic’ fashion through the peritoneal cavity, and as such there may be tumour seedlings on the peritoneal surfaces of the bowel, bladder, etc.

69
Q

Are Krukenberg tumours usually one or two sided?

A

Both

70
Q

Which tumours can metastasise to the ovaries, and what are the common patterns of spread?

A

The most common tumours are those arising from the large bowel, appendix, breast, stomach, uterus, and skin:

The most common metastases to go to the ovary are from the uterus (e.g. endometrial carcinoma) and fallopian tube (rare site of primary adenocarcinoma), and the contralateral ovary. The former are spread via the fallopian tube to the ovary, the latter will arise through transcoelomic spread.

Transcoelomic spread as described above. Common route by which gastrointestinal and breast tumours are spread to the ovary.

Lymphatics (e.g. breast, colon) and haematogenous route. The latter is usually seen late in the disease by which there are metastatic tumour deposits elsewhere.

Spread may also occur by direct extension from adjacent pelvic organs, e.g. bladder, bowel.

The prognosis for women with ovarian metastases is usually poor.

71
Q

What is is the most common malignant tumour of the female genital tract? The peak incidence is between the ages of 55-65 yrs, and it is unusual in women <40 yrs old.

A

Endometrial adenocarcinoma

72
Q

Post-menopausal bleeding. Large polypoid mass arising from the endometrium, filling the endometrial cavity. The mass is tan in colour with areas of haemorrhage and necrosis. Diagnosis?

A

endometrial carcinoma

73
Q

What are the subtypes of endometrial carcinoma?

A

The most common subtype is the endometrioid type, which is a tumour that tends to be well-differentiated, mimicking the normal endometrial glands (it is an adenocarcinoma).

The second subtype, papillary serous carcinoma (like the ovarian counterpart) is less common (10% of endometrial tumours), and it is seen in older women who have an atrophic endometrium. These serous tumours are aggressive and have a poor prognosis.

74
Q

Risk factors for endometrial carcinoma

A

These tumours develop on a background of excessive oestrogen stimulation. There is often a pre-malignant phase of atypical endometrial hyperplasia. Oestrogenic stimulation may be the result of exogenous or endogenous sources of oestrogen, for example:

  • Excessive oestrogen due to early menarche, late menopause
  • Obesity - there is an increased production of oestrogen within adipose tissue (fat) from adrenal or ovarian androgens.
  • Hormone replacement therapy - this applies only to oestrogen-only therapy
  • Tamoxifen - this is a drug used in the treatment of breast cancer. In the breast this drug has an anti-oestrogenic effect, but in the endometrium it has a pro-oestrogenic effect.
  • Anovulatory menstrual cycles (for example which may be seen in some patients with polycystic ovaries)
  • An oestrogen secreting ovarian tumour (sex-cord/stromal tumour such as thecoma, granulosa cell tumour)

Others:

  • Hypertension and type 2 diabetes are also risk factors (possibly associated with obesity)
  • Individuals with HNPCC syndrome (hereditary non-polyposis colon cancer syndrome) have a 22-50% chance of developing endometrial carcinoma.
  • There is also a 2 - 3x increased risk in individuals with a history of breast cancer.
75
Q

How could a benign ovarian tumour cause ovarian carcinoma?

A

A thecoma (ovarian tumour of sex cord/stromal origin) could secrete hormones, and if oestrogen is secreted, this will stimulate proliferation of the endometrium. This may present with irregular menstrual bleeding or postmenopausal bleeding (PMB). A small number of these individuals will develop endometrial carcinoma.

76
Q

Prognostic factors for endometrial tumours

A
  • stage of the tumour, and on the tumour grade

- type of tumour is also important; serous papillary carcinoma has a poor prognosis overall

77
Q

What’s the ovarian germ cell tumour is the exact counterpart of the seminoma arising in the male testis?

A

Dysgerminoma

78
Q

Is Dysgerminoma benign or malignant?

A

a rare malignant tumour occurring predominantly in young females

79
Q

lump in wall of uterus, uniform cream whorled cut surface

A

Leiomyoma

80
Q

Features of type 1 endometrial adenocarcinoma

A
  • 80%
  • low grade endometrioid carcinoma
  • post/perimenopausal women with higher concentrations of oestrogen
  • background of endometrial hyperplasia
  • PTEN mutations 50%
81
Q

Features of type 2 endometrial adenocarcinoma

A
  • 20%
  • uterine serous carcinoma
  • older postmenopausal women with atrophic endometrium
  • arises in a background of serous intraepithelial carcinoma
  • TP53 mutations 80-90%
82
Q

Risk factors for endometrioid endometrial carcinoma (type 1)

A
  • Post/perimenopausal women with higher total concentrations of oestrogen
  • obesity
  • diabetes
  • hypertension
  • PCOS
  • oestrogen producing tumours
  • early menarche
  • late menopause
  • nulliparity
83
Q

Morphology of endometrioid endometrial carcinoma (type 1)

A

Crowded complex proliferative glands
Gland fusion/cribriforming, cytological atypia
Solid sheets of cells
+/- squamous differentiation

84
Q

Risk factors for uterine serous carcinoma

A

Multiparous
Smokers
Less obese
History of breast carcinoma (germline BRCA1/2 mutations)

85
Q

Grading of endometrial carcinomas

A

FIGO

stage 0: carcinoma in situ
stage I: limited to the body of the uterus
Ia: no or less than half (≤ 50%) myometrial invasion
Ib: invasion equal to or more than half (≥ 50%) of the myometrium
stage II: cervical stromal involvement
endocervical glandular involvement only is stage I
stage III: local or regional spread of the tumour
IIIa: tumour invades the serosa of the body of the uterus and/or adnexa
IIIb: vaginal or parametrial involvement
IIIc: pelvic or para-aortic lymphadenopathy
IIIc1: positive pelvic nodes
IIIc2: positive para-aortic nodes with or without pelvic nodes
stage IV: involvement of rectum and or bladder mucosa and or distant metastasis
IVa: bladder or rectal mucosal involvement
IVb: distant metastases, malignant ascites, peritoneal involvement

86
Q

Cowden disease

A

PTEN mutation

Cowden’s disease and sometimes as multiple hamartoma syndrome

Rrare autosomal dominant inherited disorder characterized by multiple non-cancerous tumor-like growths called hamartomas, which typically are found in the skin, mucous membranes (mouth, nasal membranes, GI tract), thyroid gland, and breast tissue. While the hamartomas are benign, people with Cowden syndrome are at increased risk of certain forms of cancer, including breast, thyroid, uterus (endometrial), and kidney cancers.

87
Q

Lynch syndrome

A

Mis match repair mutation

88
Q

Management of uterine leiomyomas

A

Medical (progestogens, GnRH agonists)
Uterine artery embolization/ligation
Surgery: myomectomy, TCRF, histerectomy

89
Q

fibroidectomy aka

A

myomectomy

90
Q

TCRF

A

Trans cervical resection of fibroid

91
Q

What is placenta praevia and what’s the associated problem?

A

Implantation of placenta into lower uterine segment or cervix

Predisposes to massive antepartum haemorrhage and/or preterm labour

92
Q

What is placenta accreta and what’s the associated problem?

A
  • partial or complete absence of decidua
  • placenta is directly adherent to myometrium
  • predisposes to massive post partum haemorrhage
  • often associated with placenta praevia, cornual implantation, leiomyomas, uterine scarring
93
Q

Interlacing bundles of spindle cells

A

Fibroids

94
Q

What’s necrobiosis?

A

Infarction of a fibroid can cause red degeneration (necrobiosis) which presents with acute pain and fever

95
Q

What’s endometriosis and what are the subtypes?

A

Presence of endometrial glands and stroma outside the uterus

Metastatic- menstrual regurgitation through fallopian tube, lymphatic or vascular

Metaplastic- secondary mullerian system of peritoneum

Neoplastic- ovarian endometrioid cystadenoma

96
Q

Common sites for endometriosis

A

Ovary and tubes (80%)
Uterine ligaments
Recto-vaginal septum
Pelvic peritoneum

97
Q

‘large for dates’ uterus and bleeding in early pregnancy, can cause abortion in late 1st or 2nd trimester, histology: abnormal trophoblast proliferation and swollen chorionic villi

A

Hydatidiform mole

98
Q

What causes excessive vomiting (hyperemesis) associated with hydatidiform mole?

A

high beta-HCG levels

99
Q

ultrasound scan showing grape-like clusters of vesicles and a uterine evacuation

A

Hydatidiform mole

100
Q

What is a hydatidiform mole?

A

Abnormal proliferation of pregnancy-associated trophoblastic tissue associated with villous hydrops

101
Q

Incidence of hydatidiform moles

A

1 per 1000 pregnancies

102
Q

Risk factors for hydatididform moles

A

Maternal age < 15 years, > 40 years

103
Q

Types of moles

A

Complete
A complete mole is caused by a single (incidence is about 90%) or two (incidence is about 10%) sperm combining with an egg which has lost its DNA (the sperm then reduplicates forming a “complete” 46 chromosome set). No fetus

Partial
a partial mole occurs when a haploid egg is fertilized by two sperm or by one sperm which reduplicates itself yielding the genotypes of 69,XXY (triploid) or 92,XXXY (tetraploid).

104
Q

Management of moles

A
  • Confirm diagnosis (looking for paternally imprinted genes e.g p57 by IHC)
  • Refer to trophoblastic unit
  • Follow up with serial betaHCG measurements
105
Q

Persistent gestational trophoblastic disease (if mole doesn’t spontaneously abort)

A
  1. An invasive mole shows invasion of the myometrium and the main complication is uterine perforation.
  2. Choriocarcinoma is a rare highly malignant neoplasm which metastasises via the blood stream. However, it is exquisitely sensitive to chemotherapy. About half of choriocarcinomas develop from a preceeding hydatidiform mole (hence the importance of diagnosis and follow up), the other half develop after a normal pregnancy or nonmolar miscarriage.
106
Q

Where do choriocarcinomas metastasize to?

A

Lungs
Brain
Liver

107
Q

Where abouts in the cervix is a smear test done?

A

The transformation zone

108
Q

What’s the transformation zone?

A

An area around the cervical os in which the cells are most susceptible to infection with HPV and therefore to dysplastic changes which may progress to invasive malignancy.

109
Q

Which area undergoes natural metaplasia?

A

TZ.
From columnar mucosa of the endocervix to the more robust squamous epithelium of the ectocervix as a result of exposure to the acidic environment of the vagina.

110
Q

The amount of endocervical columnar epithelium present outside the endocervical canal depends on what?Where is the squamocolumnar junction before and after puberty and post menopause?

A

Hormonal control

Before puberty: within endocervical canal

After puberty: into cervix (cervical ectropion)

Postmenopause: TZ recedes into the endocervical canal

111
Q

Where does squamous carcinoma of the cervix arise?

A

TZ

112
Q

Low power: squamous epithelial cells appear crowded together
High power: epithelium appears disorganised and shows loss of normal maturation. Nuclei are large, irregular and hyperchromatic, mitotic figures at the basal layer of the epithelium

A

CIN3 (cervical intraepithelial neoplasia)

113
Q

What’s the term for ‘epithelial cells in the superficial layers of the epithelium, have irregular and angulated nuclei around which the cytoplasm is cleared’

A

Koilocytes

Classic of epithelial cells infected with HPV

114
Q

Risk factors for developing CIN

A
  • Unprotected sex
  • number of sexual partners
  • oral contraceptive
  • early age at first intercourse
  • immunosuppression
115
Q

Low risk HPVs and what do they cause?

A

6,11

Flat warts, benign

116
Q

High risk HPVs 16, 18, 31

A

Associated with CIN and cervical cancer

117
Q

Pathogenesis of HPV and CIN

A

E6 oncoprotein of the HPV16 and 18 binds to tumour suppressor gene p53 and accelerates its proteolytic degradation. E7 oncoprotein binds to the RB gene and displaces transcription factors normally sequestered by this gene. Affect cell cycle

118
Q

Koilocytes in upper layers (virus in differentiated cells), crumpled irregular nuclei with perinuclear halos, dyskeratosis and multinucleation.

A

High risk HPV

119
Q

How does the HPV vaccine work?

A

Prophylactic (immune response against L1 genes, capsid proteins)

Prevent against associated conditions

120
Q

What does CIN stand for?

A

Cervical intraepithelial neoplasia

121
Q

What does LSIL stand for?

A

Low grade squamous intraepithelial lesion

122
Q

What does HSIL stand for?

A

High grade squamous intraepithelial lesion

123
Q

Features of LSIL

A

CIN I/LISL

Replacement of the basal third of the epithelium by tumour cells (previously called mild dysplasia)

124
Q

Features of HSIL

A

HSIL includes CIN II and CIN III

CIN II
Abnormal cells extend into the middle third, previously called moderate dysplasia.

CIN III
Abnormal cells extend into the upper third, previously called severe dysplasia or carcinoma in situ.

125
Q

What happens if low grade abnormalities (smears showing HPV changes and mild dyskaryosis) are detected?

A

Tested for presence of high risk HPVs

126
Q

What happens if high grade dyskaryosis (moderate and severe) are detected?

A

Referred for colposcopy and maybe biopsied prior to treatment

127
Q

Who gets a smear test?

A

Women 25-64
Every 3 years up to 49 years
Every 5 years over 50

128
Q

What’s an LLETZ?

A

A large loop excision of the transformation zone

129
Q

How is a LLETZ done?

A

A LLETZ is a procedure to remove cervical tissue for examination and to treat some precancerous changes of the cervix.

A thin wire loop heated by an electrical current is used like a scalpel to remove the abnormal tissue from the transformation zone of the cervix. Sometimes the doctor can remove all visible abnormal cells.

A LLETZ is usually done under a local anaesthetic in the doctor’s office or, sometimes, under a general anaesthetic in hospital. It takes about 10 minutes. Sometimes it is done at the same time as a colposcopy and biopsy.

Once the tissue sample has been taken, it will be sent to a laboratory for examination under a microscope. The results will be available in about a week.

130
Q

CIN vs CGIN

A

CIN: Cervical intraepithelial neoplasia
Squamous cells

CGIN: Cervical Glandular Intra-epithelial Neoplasia
Glandular cells

131
Q

Who is at risk of clear cell carcinoma?

A

Seen in young patients (15-20 years) whose mothers were exposed to diethylstilbestrol during pregnancy to prevent spontaneous abortions.

132
Q

Risk factors for cervical carcinoma

A
  • Unprotected sex
  • number of sexual partners
  • oral contraceptive
  • early age at first intercourse
  • immunosuppression
  • smoking
133
Q

Following a diagnosis of CIN3 a patient has the area removed. What happens next?

A
  • smear test at 6 months
  • if negative or shows low grade changes HPV testing will be performed (Test of cure)
    if positive patient will undergo another colposcopy
134
Q

What’s the most common malignancy to arise in the cervix?

A

Squamous cell carcinoma 60-80 %

Adenocarcinoma 2nd

135
Q

What’s the relationship between CIN3 and squamous cell carcinoma?

A

CIN is the precursor.

Only 15% of CIN1 progresses to CIN2-3 and untreated CIN2-3 is associated with a 22-72% risk of developing invasive carcinoma.

136
Q

Most important risk factor associated with cervical carcinoma?

A

Never having had a smear test!

137
Q

Risk factors for endometrial adenocarcinoma

A 
Tamoxifen
HRT
Obesity
T2DM
Hypertension
Genetic factors (Lynch syndrome, Cowden)
138
Q

18 weeks of amenorrhoea, ‘large for dates’ uterus on ultrasound and no fetus, placental tissue is composed of fluid-filled vesicles, villi of varying sizes, proliferating trophoblasts.

A

Complete hydatidiform mole

139
Q

Complications following a hydatidiform mole

A

Persistent mole

Choriocarcinoma

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